Rotavirus Infects

Rotavirus infects mature endothelial cells at the tip of the villi, which are present in the lumen of the small intestine. Prior to infection, the VP4 spike protein was cleaved into VP5 * 75, the body of the spike protein, and VP8 *, the head of spike proteins, by proteolysis with trypsin-like proteases present in the small intestine 75. In the endoplasmic reticulum, a cascade of processes is little known, with the assembly of VP4 and VP7 on the double layer particle and the removal of the transient envelope. VP7 also participates in the removal of the transient membrane as shown to block VP7 membranes in vitro. The release of the cell is possible by two mechanisms: cell lysis and secretion of the apical cell surface. Rotavirus replication takes place in the
The non-structural protein 4 of the rotavirus toxin has been shown to be released very early during infection 34, first as a cleavage product comprising the toxic region released from the infected cells, beginning 4 hours after infection 82 and Later during infection as a non-structural glycosylated protein 4 18. Virus that binds to the cell surface by VP4 or the VP8 cleavage product 75. The conformational change is protease-dependent, with VP4 being cleaved in VP8 and VP5 75. Rotavirus has a tropism for mature enterocytes, but the exact receptor for viral binding in vivo has not yet been identified, although sialic acid, integrins 33, histo-blood group antigens and toll receivers have been proposed 1181. Cell initiation by receptor-mediated endocytosis occurs through VP5, indicating that excision of VP4 in VP5 and VP8 is required 77. Calcium-dependent endocytosis was also demonstrated, and non-clathrin, non-caveolin dependent endocytosis provides the virion to the early